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1 Centre for Musculoskeletal Research, University of Gävle, PO Box 7629, S-907 12 Umeå, Sweden2 Department of Movement Physiology, Bogomoletz Institute of Physiology, National Academy of Sciences, Bogomoletz Street 4, 01024 Kiev, Ukraine3 Department of Neurophysiology, Institute for Medical Research, PO Box 102, Belgrade, Serbia and Montenegro4 Department of Surgical and Perioperative Science, Sport Medicine Unit, Umeå University, Umeå, Sweden, S-901 87
In decerebrate cats, changes in the monosynaptic reflex (MSR) of gastrocnemius–soleus (G–S) motoneurones were studied after fatiguing stimulation (FST) of the G–S muscles. Monosynaptic reflexes were evoked by stimulation of Ia fibres in the G–S nerve and recorded from a filament of ventral root (VR) L7. FST (intermittent 40 s–1 stimulation for 10–12 min) was applied to the distal part of the cut VR S1. FST reduced MSR amplitudes to 0.64 ± 0.04 (mean ±S.E.M.) of the prefatigue values. The suppression remained stable for approximately 25 min and then MSR amplitudes gradually returned towards the normal. To test for the involvement of presynaptic and recurrent inhibition, MSRs were conditioned by stimulation of the nerve to the posterior biceps and semitendinosus (PBSt) muscles or a filament of VR L7, respectively. The intensity of presynaptic inhibition (reduction of the normalized value of MSR amplitude during conditioning) increased from 0.19 ± 0.02 in prefatigue to 0.44 ± 0.04 within a 5.3–18.2 min interval after FST, followed by a recovery. In contrast, the intensity of recurrent inhibition first diminished from 0.23 ± 0.02 in prefatigue to 0.15 ± 0.01 within 15.6–30.1 min after FST and then gradually recovered. Both primary afferent depolarization and the intensity of antidromic discharges in primary afferents increased with the presynaptic inhibition intensity. These results demonstrate a fatigue-related suppression of Ia excitation of synergistic motoneurones, probably arising from the activation of group III and IV afferents. The effects could in part be due to increased presynaptic inhibition, while recurrent inhibition plays a minor role.
(Received 10 August 2003;
accepted after revision 21 November 2003;
first published online 28 November 2003)
Corresponding author I. Kalezic: Centre for Musculoskeletal Research, University of Gävle, PO Box 7629, S-907 12 Umeå, Sweden. Email: ivana.kalezic{at}hig.se
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